Morus alba Leaf Extract Attenuates Glyphosate-Induced Oxidative Stress, Inflammation and Alleviates Liver Injury in Rats

2022 ◽  
Vol 18 (1) ◽  
pp. 24-35
Author(s):  
El Hafedh El Mouhab ◽  
Olfa Rebai ◽  
Sami Zekri ◽  
Lamia Charfi ◽  
Sadok Boukhchina ◽  
...  
2018 ◽  
Vol 21 (9) ◽  
pp. 899-904 ◽  
Author(s):  
Derya Ustuner ◽  
Emine Colak ◽  
Murat Dincer ◽  
Neslihan Tekin ◽  
Dilek Burukoglu Donmez ◽  
...  

Author(s):  
Arezoo Ahmadi ◽  
Esfandiar Heidarian ◽  
Keihan Ghatreh-Samani

Abstract Background Diazinon (DZN) causes serious liver damage in both humans and animals. In the present study, the hepatoprotective effects of Cynara scolymus L. leaf extract against DZN-induced liver injury were examined. Methods Forty male rats were divided into five groups. The control group received a normal diet. The DZN group received DZN only (25 mg/kg, po). The DZN + Syl group received DZN (25 mg/kg, po) and silymarin (Syl) (50 mg/kg, po). The DZN + Art group received DZN (25 mg/kg, po) and artichoke (Art) leaf extract (1500 mg/kg, po). The Art group received Art leaf extract only (1500 mg/kg, po). After 15 days, serum tumor necrosis factor α (TNF-α), alanine aminotransferase (ALT), aspartate aminotransferase (AST), alkaline phosphatase (ALP), lipid profile, protein carbonyl content, serum and hepatic malondialdehyde (MDA), hepatic TNF-α gene expression, hepatic catalase (CAT), superoxide dismutase (SOD), and vitamin C (Vit C) were measured and histopathological examination was performed. Results DZN caused a significant elevation in serum ALP, AST, ALT, MDA, TNF-α, protein carbonyl, hepatic MDA, and TNF-α gene expression in the DZN group as opposed to the control group. Also, DZN led to the reduction of hepatic CAT, SOD, and Vit C in the DZN group relative to the control group. The administration of Art extract resulted in not only a significant reduction in serum ALP, AST, ALT, MDA, TNF-α, and protein carbonyl but also an improvement of liver histopathological changes and hepatic CAT and SOD activities as opposed to the DZN group. Conclusions This study confirmed that Art leaf extract has liver protective effects and causes downregulation of oxidative stress in acute DZN-induced liver injury in rats.


Author(s):  
Bin Wang ◽  
Gaurav Gupta ◽  
Mahaveer Singh ◽  
Kasturi Vishwanatha Setty Veerabhadrappa ◽  
Anurag Mishra ◽  
...  

2020 ◽  
Vol 10 (4) ◽  
pp. 384-394
Author(s):  
Sainiara Begum ◽  
Archana Banerjee ◽  
Bratati De

Aims:The foliar residues of Mangiferaindica tree are usually burned or used for soil amelioration except nominal uses as fodder.Methods:To add value to this agricultural waste, extracts of the leafy residues of M. indica were studied to analyze their potential as antioxidants and to inhibit the enzymes related to the management of diabetes, Alzheimer’s Disease (AD), hepatic disorders as well as to identify important phytochemicals present in the extracts.Results:Results depicts that the leaves have notable bioactivities. The methanol extract (ME) showed much potential than ethyl acetate fraction after hydrolysis (HME) against α-amylase and α- glucosidase. The activity against the enzyme β-glucuronidase was also higher than that of the commercial β- glucuronidase inhibitor. The extract after hydrolysis showed better antioxidant and acetylcholinesterase inhibitory activities. Detection of important phytochemicals such as chrysin and myricetn, alizarin, arbutin, hydroquinone, tyrosol, taxifolin, kaempferol, mangiferin, and the vitamin alpha tocophereol, in addition to a number of organic acids, amino acids, fatty acids, sugars and polyols by GC-MS and HPTLC based analysis of the extract of M. indica leaf, also suggest the use of the leaves as sources of these important phytochemicals.Conclusion:More concisely HME with more number of detected metabolites found better to be used against oxidative stress as well as enzymes related to neural and liver disorders than that of ME.


Author(s):  
Shipra Bhatt ◽  
Ankita Sharma ◽  
Ashish Dogra ◽  
Priyanka Sharma ◽  
Amit Kumar ◽  
...  

2021 ◽  
Author(s):  
Xinling Song ◽  
Wenxue Sun ◽  
Wenxin Cai ◽  
Le Jia ◽  
Jianjun Zhang

A polysaccharide named as PFP-1 was isolated from Pleurotus geesteranus fruiting body, and the potential investigations on ameliorating oxidative stress and liver injury against alcoholic liver disease (ALD) were processed...


2021 ◽  
Vol 27 (1) ◽  
Author(s):  
Da Tang ◽  
Guang Fu ◽  
Wenbo Li ◽  
Ping Sun ◽  
Patricia A. Loughran ◽  
...  

Abstract Background Hepatic ischemia/reperfusion (I/R) injury can be a major complication following liver surgery contributing to post-operative liver dysfunction. Maresin 1 (MaR1), a pro-resolving lipid mediator, has been shown to suppress I/R injury. However, the mechanisms that account for the protective effects of MaR1 in I/R injury remain unknown. Methods WT (C57BL/6J) mice were subjected to partial hepatic warm ischemia for 60mins followed by reperfusion. Mice were treated with MaR1 (5-20 ng/mouse), Boc2 (Lipoxin A4 receptor antagonist), LY294002 (Akt inhibitor) or corresponding controls just prior to liver I/R or at the beginning of reperfusion. Blood and liver samples were collected at 6 h post-reperfusion. Serum aminotransferase, histopathologic changes, inflammatory cytokines, and oxidative stress were analyzed to evaluate liver injury. Signaling pathways were also investigated in vitro using primary mouse hepatocyte (HC) cultures to identify underlying mechanisms for MaR1 in liver I/R injury. Results MaR1 treatment significantly reduced ALT and AST levels, diminished necrotic areas, suppressed inflammatory responses, attenuated oxidative stress and decreased hepatocyte apoptosis in liver after I/R. Akt signaling was significantly increased in the MaR1-treated liver I/R group compared with controls. The protective effect of MaR1 was abrogated by pretreatment with Boc2, which together with MaR1-induced Akt activation. MaR1-mediated liver protection was reversed by inhibition of Akt. Conclusions MaR1 protects the liver against hepatic I/R injury via an ALXR/Akt signaling pathway. MaR1 may represent a novel therapeutic agent to mitigate the detrimental effects of I/R-induced liver injury.


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